Hypoxia increases production of interleukin-1 and tumor necrosis factor by human mononuclear cells
| Autor: | Carl W. White, John E. Repine, Pietro Ghezzi, Marina Bianchi, Mary E. Rosandich, Charles A. Dinarello |
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| Rok vydání: | 1991 |
| Předmět: |
Lipopolysaccharides
medicine.medical_specialty ARDS Immunology Radioimmunoassay Biochemistry Peripheral blood mononuclear cell Proinflammatory cytokine Internal medicine Immunology and Allergy Medicine Humans RNA Messenger Hypoxia Molecular Biology Cells Cultured L-Lactate Dehydrogenase business.industry Septic shock Tumor Necrosis Factor-alpha Interleukin Hematology Hypoxia (medical) medicine.disease Endotoxins Endocrinology Tetradecanoylphorbol Acetate Leukocytes Mononuclear Tumor necrosis factor alpha medicine.symptom business Interleukin-1 |
| Zdroj: | Cytokine. 3(3) |
| ISSN: | 1043-4666 |
| Popis: | Exposure to hypoxia (PO2 = 9 +/- 1 torr) increased human peripheral blood mononuclear cell production and secretion of interleukin-1 (IL-1)alpha, IL-1 beta, and tumor necrosis factor (TNF) percent of control = 190% for IL-1 alpha, p = 0.014; 219% for IL-1 beta, p = 0.014; and 243% for TNF, p = 0.037) following treatment with endotoxin (1 ng/ml). Hypoxia potentiated the increased production of these inflammatory cytokines at subthreshold levels of endotoxin with potentiation increasing at lower O2 concentrations. Hypoxia also increased cytokine production induced by the tumor promoter phorbol myristate acetate, suggesting a generalized biologic response. We conclude that hypoxia increases IL-1 and TNF production and speculate that this mechanism aggravates a variety of pathologic conditions involving endotoxin such as adult respiratory distress syndrome (ARDS), multiple organ failure, and septic shock. |
| Databáze: | OpenAIRE |
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